Lyme disease | DermNet New Zealand DermNet New Zealand Author: Vanessa Ngan, Staff Writer, 2003. Updated by Dr Daniela Vanousova, Dermatologist, Czech Republic, March 2015. What is Lyme disease? Lyme disease is an infection caused by borrelia, a type of bacteria called a spirochaete. Lyme disease can affect any part of the body, most commonly skin, central nervous system, joints, heart, rarely eyes and liver. Lyme disease is common in parts of the United States (particularly in Massachusetts) and in Europe, but is reported from many areas of the world. In New Zealand, cases have only been reported in people that have recently travelled from an endemic area. Lyme disease is also called Lyme borreliosis. What are the subtypes of Lyme disease? There are different types of borrelia in each continent resulting in different forms of Lyme disease in North America and Europe.

In North America, the infection is due to the subspecies B burgdorferi sensu stricto and most often presents as: Erythema migrans Lyme arthritis In Europe, the infection is due to the subspecies B burgdorferi sensu stricto, B afzelii and B garinii, and most often presents as: Erythema migrans Acrodermatitis chronica atrophicans (due to B afzelii) Lyme neuroborreliosis How do you catch borrelia infection? Humans and animals are infected with the bacteria through hard-tick bites. The borrelia bacteria survive in the midgut of the ticks. The immature nymphs are most likely to transmit the infection. The ticks feed on infected animals and then on humans. Ticks occur in high grass, brush, woodland and leafy forest. The main hosts for the ticks and borrelia are small to medium-sized animals in Europe and deer in North America.

In North America, the tick vectors are Ixodes scapularis, I pacificus, and 4 other tick species In Europe and Asia, the tick vectors are I ricinus, I hexagonus, and I persulcatus Who gets Lyme disease? Lyme disease can affect children and adults. Infection most often occurs in forestry workers and in those who have been enjoying recreational activities in areas where ticks reside. What happens after a tick bite? Ticks can attach and feed in any part of the human body. The bite is painless. Because they are very tiny (just 2 mm in size) nymph bites are often overlooked. Borrelia are transmitted from the midgut of the infected tick to the attached skin when attachment lasts for 36–48 hours. Several things can happen after being bitten by an infected tick. The body's defence mechanisms can overwhelm and eliminate the infecting bacteria. The bacteria can remain localised at the site of the bite and cause a localised skin infection. The bacteria may disseminate via the blood and lymphatic system to other organs and cause a multisystem inflammatory disease. Erythema chronicum migrans What are the signs and symptoms?

The disease can basically be divided into 3 stages according to the extent of infection.

Stage 3–33 days after tick bite Erythema migrans 'Flu-like illness with low-grade fever, chills, fatigue and joint pain Borelial lymphocytoma – red to blue patch on the earlobe, nipple or scrotum, (common in childrem) Early disseminated Lyme disease Days to weeks after tick bite Multiple eythema migrans, smaller than initial patch Early neuroborreliosis Facial or Bell palsy – one sided paralysis of the facial muscles (common in children) Aseptic meningitis – fever, severe headaches and neck stiffness Polyradiculitis – numbness and pain in arms or legs Other cranial nerve palsies, mild encephalitis, peripheral neuritis Arthritis – painful and swollen large joints (knee is the most affected join) Carditis – abnormal heart rate Progression is gradual over months to years Progression is gradual over months to years Late Lyme disease Chronic Lyme arthritis (chronic severe joint pain and swelling) in one or more large joints, mostly knee (more common in North America than in Europe) Chronic neurological disorders such: Disorientation, confusion, dizziness, lack of concentration, short-term memory loss Shooting pain, numbness extending to hands/arms

 and feet/legs Erythema migrans Erythema migrans, a red expanding patch of skin, is the most typical sign of Lyme disease and is present in 70–80% of cases.

It usually appears 7–14 days (range 3–33 days) after the infected tick bite. It starts at the site of the tick bite as a red papule or macule that gradually expands. The size of the rash can reach several dozens of centimetres in diameter. A central spot surrounded by clear skin that is in turn ringed by an expanding red rash (like a bull's-eye) is the most typical appearance. Erythema migrans may also present as a uniform erythematous patch or red patch with central hardening and blistering. The redness can vary from pink to very intensive purple. Erythema migrans is mostly asymptomatic, but can be itchy, sensitive or warm if touched. It is rarely painful. Fatigue, chills, headache, low-grade fever, muscle and joint pain, may occur briefly and then recur if the disease progresses. Lymph glands near the tick bite may be swollen. Erythema migrans disappears spontaneouslly within 3–4 weeks. If left untreated the disease may disseminate, affect other organs, and progress to the next stage.

Diagnosis of Lyme disease It is important to get early diagnosis if you think you may have Lyme disease. Diagnosis can be made on the presence of erythema migrans and other symptoms, plus a history of or evidence of a tick bite. Laboratory tests are usually not necessary in the early stage of erythema migrans, Undetected or ignored early symptoms may be followed by more severe symptoms weeks, months or even years after the initial infection. Certain laboratory tests are then recommended to confirm diagnosis and should be interpreted by an expert.. Antibody titres to B burgdorferi using enzyme-linked immunoassay (ELISA) or immunofluorescent assay. Positive results should be confirmed by Western immunoblot Acrodermatitis chronica atrophicans The organism can be cultured and/or polymerase chain reaction (PCR) test for the organism can be done on the skin specimen Positive antibodies to B. burgdorferi can be in many cases detected for many years after the successful treatment. Tick bites may transmit other infections like tick-born encephalitis, anaplasmosis and babesiosis.

Co-infections should be considered if symptoms of Lyme disease are severe or prolonged, in case of high fever, and abnormal blood tests results (leucopaenia, thrombocytopenia, elevation of liver transaminases). What treatment is available for Lyme disease? Localised or early Lyme disease generally responds well to appropriate antibiotics. Full cure is usually achieved if the disease is diagnosed and treated promptly, but the cure rate decreases the longer treatment is delayed. The choice of antibiotic depends on bacterial sensitivity. Antibiotics used include, doxycycline , amoxicillin, cefuroxime, azithromycin, erythromycin , intravenous penicillin and cetriaxone. The route of administration and the duration of antibiotic course depends on the stage and organ involvement. It varies between 10 and 30 days. Late stage Lyme disease, especially neuroborreliosis, should be treated with intravenous antibiotics. Some patients have persistent or recurrent symptoms of unknown origin after apparently successful antibiotic treatment for Lyme disease. This is called post-treatment Lyme borreliosis syndrome. It is believed to be an auto-immune response. Prolonged antibiotic treatment does not improve cure rates.

Prevention of Lyme disease Avoid areas endemic for Lyme borreliosis. When walking in high grass or woodland, wear white clothes (so the tick can be seen more easily) with long sleeves, long trousers tucked into socks, or long boots. Use repellents/pesticides. After return from a walk in an endemic area, change your clothes and check your whole body carefully. The next day, check your body for ticks again. Remove the tick as a prompt removal decreases the risk of Lyme disease transmission. Disinfect the site. Use tweezers to carefully and steadily pull the tick out from the skin. Disinfect the site again. Wash your hands. Watch the site of the tick bite for several weeks. If a rash appears bigger than 5 cm or you have 'flu-like symptoms, consult your doctor. There is no vaccine for Lyme disease. Related information References: Textbook of Dermatology. Ed Rook A, Wilkinson DS, Ebling FJB, Champion RH, Burton JL. Fourth edition. Blackwell Scientific Publications. On DermNet NZ: Erythema | University of Maryland Medical Center Medications, such as birth control pills; sulfa drugs Who is Most At Risk?

Men are at greater risk than women for erythema multiforme. Women are at greater risk than men for erythema nodosum. Frequent or excessive sun exposure increases the risk for erythema multiforme. People between 20 to 30 years of age are at greater risk of erythema nodosum. People with a family history of skin conditions have a greater chance of developing either erythema multiforme or erythema nodosum.

Signs and Symptoms Fatigue, fever, and itching (before lesions appear) Sudden outbreak of spots, bumps, and lesions (usually on knees, elbows, palms, hands, and feet) Target lesions (spots surrounded by rings of normal and red skin, looking like a target) Erythema infectiosum (caused by a virus and known as fifth disease), rash on face and arms lasting about 2 weeks Erythema nodosum: Fatigue, flu-like symptoms (before lesions appear) Clusters of nodules (small round masses) and lesions on shins, forearms, thighs, and trunk Red, painful lesions become soft and bluish, and fade to yellow and brown Joint pain Arthritis Stevens-Johnson syndrome (SJS) and toxic epidermal necrolysis (TEN), the most severe forms of erythema multiforme, have a different set of symptoms. Target lesions on the trunk, hacking cough, fever, and blisters around the mouth, eyes, nostrils, and anal and vaginal areas are the key symptoms of SJS.

A person with TEN will have symptoms of SJS that worsen to include peeling and detachment of the skin, pus-like infections, fluid loss, and even death. What to Expect at Your Doctor's Office Your doctor will perform a physical exam and may order a skin biopsy, throat culture, blood test, or x-ray to determine the type of erythema. These tests also may reveal any infections or medications that are contributing to symptoms. Treatment Options Prevention Treat underlying diseases and avoid known triggers (certain medications, for example). It is also important to avoid the sun when taking certain medications. Treatment Plan Your doctor will treat any underlying diseases, stop any drugs that may contribute to symptoms, and take steps to control your current symptoms. Mild cases may not require treatment. Bed rest and medication may be necessary for more severe cases. Drug Therapies Antihistamines for itching Antibiotics.

If you have an infection, though research suggests many cases of erythema can be resolved without antibiotics Antiviral medications such as acyclovir and valacyclovir, if you have a virus Aspirin and nonsteroidal anti-inflammatory drugs (NSAIDs) Burrow's compresses, a solution used to soothe skin conditions, particularly blisters Corticosteroids, applied to the skin (topically); corticosteroids may also be taken orally to reduce symptoms of erythema nodosum Intravenous immunoglobulin, used experimentally for SJS and TEN Photomodulation therapy, use of a light-emitting diode to accelerate the resolution of erythema Complementary and Alternative Therapies To treat erythema, you must treat the underlying cause. It is important to get a proper diagnosis from your doctor before using complementary and alternative therapies (CAM). Not all CAM therapies are appropriate for all people, and some may interact with conventional medicines or therapies. You should use CAM therapies only under the guidance of a physician. Some CAM therapies may be used to: Reduce inflammation Prevent infections Nutrition Antioxidants are molecules that scavenge free radicals (chemicals that can damage cells).

Antioxidants also may protect skin against damage caused by ultraviolet (UV) sun rays. The following antioxidants have been shown to protect skin against damage in scientific studies: Beta-carotene and other carotenoids (up to 300 IU per day for beta-carotene): Beta-carotene is often used as a standard treatment for sun sensitivity, although studies have been mixed. In one trial, though, 20 healthy subjects received either carotenoids alone, mainly from beta-carotene, or carotenoids plus vitamin E. Both groups improved significantly, but vitamin E did not appear to add any benefits. Scientists think the protective effect of beta-carotene comes from its antioxidant effect, so it's possible other antioxidants may also help protect skin from damage. Vitamin B6 (100 mg per day for 3 months): Some case reports suggest that vitamin B6 can help reduce the reaction to sunlight. You should only take high doses of vitamin B6 under a doctor's supervision, because of the risk of side effects.

Vitamin B6 can interfere with Amiodarone (Cordarone), Phenobarbital (Luminal), Phenytoin (Dilantin), and possibly Levodopa. Speak with your physician if you are taking any of these medications. Vitamin C (1 to 3 g per day, lower dose if diarrhea develops): Vitamin C is an antioxidant, so it may provide some protection against skin damage from sunlight. Vitamin C can negatively impact certain health conditions, and can interfere with some medications. Speak with your physician. Vitamin E: Vitamin E is also an antioxidant, and a few studies have shown that it can offer protection from sun damage to skin when taken with vitamin C (but not alone). However, other studies have not found the same results. Vitamin E may interact with certain medications, including but not limited to, blood-thinning medications, such as warfarin (Coumadin). It may also have negative effects on people with bleeding disorders, head and neck cancers, Retinitis Pigmentosa, and other conditions. Vitamin D: In animal studies, vitamin D helped protect against damage from UVB rays. It is not clear yet whether vitamin D supplements may protect humans in the same way.

Vitamin D can interact with some medications, including but not limited to, Digoxin and Verapamil. It may also have a negative impact on some health conditions. Speak with your physician. Other Supplements Melatonin: Applying melatonin topically (either alone or in combination with vitamin E) seems to offer some protection against sunburn in healthy people, but it is not known whether melatonin also lessens effects in people prone to erythema. Zinc: Zinc is necessary for healthy skin and was used in a study along with other prescription medications as a treatment for a severe form of erythema multiforme similar to TEN. In the study, 5 out of 8 people treated with zinc showed a benefit. Because high doses of zinc can be dangerous, many doctors suggest doses below 50 mg per day. Talk to your doctor to determine which dose is right for you. Zinc can interact with certain antibiotics, Cisplatin, Amiloride, and Penicillamine (used for Wilson syndrome and Rheumatoid arthritis). Herbs Flavonoids: Some of these plant-based antioxidants may protect skin from sun damage in healthy people.

In one study, German researchers found that drinking high flavonol cocoa offered protection from the sun (the cocoa used was a special formulation that is not available commercially). In another study, pomegranate fruit extract helped protect skin cells in a test tube from UV light. It is not yet known whether taking the extract would provide any benefit. However, adding fruits and vegetables to your diet to eat more flavonoids may help. You can also take these flavonoids in dried extract form. Speak with your physician first, since certain flavonoids can interact with prescription medications: Catechin, quercetin, hesperidin, and rutin. Rose hips (Rosa canina) are also high in flavonoids and may be used as a tea. Drink 3 to 4 cups per day. Hesperidin methyl chalcone is a water-soluble form of quercetin that may act as an antihistamine. Green tea (Camellia sinensis) may also protect against erythema caused by UV light because it contains antioxidants. Herbs traditionally used topically to heal damaged skin, promote lymph circulation, and possibly treat the underlying cause of various skin conditions may be helpful.

You should check with your doctor before using any of these remedies. Some examples include: Aloe vera: Used topically for skin inflammation. One study found that aloe vera displayed anti-inflammatory effects superior to 1% hydrocortisone gel. Burdock root (Arctium lappa): Used topically for skin inflammation and wound healing. Never apply to an open wound. Calendula (Calendula officinalis): Used topically for burns, wounds, and other skin conditions. Never apply to an open wound. Goldenseal (Hydrastis canadensis): Used for infections, including those causing skin lesions. Lemon balm (Melissa officinalis): Can be applied to HSV lesions as a cream or a wash. Sage extract: Applied topically to reduce inflammation. In one study, sage extract significantly reduced the ultraviolet induced erythema to a similar extent as hydrocortisone. Slippery elm (Ulmus fulva): Applied topically, in combination with goldenseal root. Never apply to an open wound. Yarrow (Achillea millefolium): Applied topically for skin inflammation and wound healing. Never apply to an open wound.

Homeopathy Although few studies have examined the effectiveness of specific homeopathic therapies, professional homeopaths may consider the following remedies for the treatment of erythema based on their knowledge and experience. Before prescribing a remedy, homeopaths take into account a person's constitutional type, includes your physical, emotional, and psychological makeup. An experienced homeopath assesses all of these factors when determining the most appropriate treatment for an individual. Apis mellifica: For skin rashes that feel hot and dry and are sensitive to touch; may be accompanied by sore throat. Symptoms are relieved by cool drinks and baths and worsened by heat and warm liquids. This remedy is most appropriate for individuals who often feel sad, disappointed, or even depressed. They tend to cry easily, but may also be irritable and envious by nature. They are also not thirsty but may crave milk. Calendula: For burns and skin lesions that are fairly superficial. This remedy is often used after the acute phase of the skin condition has subsided to aid in complete recovery. Rhus toxicodendron: Used for blisters and vesicles accompanied by intense itching that worsens at night and improves with the application of heat.

This remedy is most appropriate for individuals who are generally restless and unable to get comfortable at night. Sulphur: For skin disorders that are accompanied by fever and intense itching. This remedy is most appropriate for individuals who are thirsty, irritable while sick, lazy, and messy under ordinary circumstances, and who describe a sensation of internal heat and burning. Symptoms tend to improve with open, cold air and worsen with warmth. Prognosis/Possible Complications When treated properly, signs and symptoms of erythema multiforme usually disappear within 4 to 6 weeks. Symptoms of erythema nodosum, however, may reappear for up to 2 years. Symptoms of SJS typically disappear in a month, but when the condition is not treated properly it may lead to blindness. Both SJS and TEN can cause death. If the drug causing either SJS or TEN is identified quickly, a person's chance of survival significantly improves. Following Up Your doctor will monitor fluid and electrolyte levels, protein loss, and any organ damage. People with erythema multiforme may need treatment in a hospital burn unit if 20% or more of their body is affected.

Special Considerations If a pregnant woman develops erythema infectiosum (fifth disease), the virus can infect the fetus and cause fetal anemia, heart failure, hydrops (collection of watery fluid), and even death. Studies have also shown that pregnancy may trigger erythema nodosum. Supporting Research Beers MH, Porter RS, et al. The Merck Manual of Diagnosis and Therapy. 18th ed. Whitehouse Station, NJ: Merck Research Laboratories; 2006:1642-1644. Blumenthal M, Goldberg A, Brinckmann J, eds. Herbal Medicine: Expanded Commission E Monographs. Newton, Mass: Integrative Medicine Communications; 2000:230-239, 253-263, 419-423. Bolognia: Dermatology. 3rd ed. St. Louis, MO: Elsevier Saunders; 2012. Chen CW, Tsai TJ, Chen YF, Hung CM. Persistent erythema multiforme treated with thalidomide. Am J Clin Dermatol.

2008;9(2):123-7. Dreher F, Denig N, Gabard B, Schwindt DA, Maibach HI. Effect of topical antioxidants on UV-induced erythema formation when administered after exposure. Dermatology. 1999;198(1):52-55. Dreher F, Gabard B, Schwindt DA, Maibach HI. Topical melatonin in combination with vitamins E and C protects skin from ultraviolet-induced erythema: a human study in vivo. Br J Dermatol. 1998;139(2):332-339. Eberlein-König B, Placzek M, Przybilla B. Protective effect against sunburn of combined systemic ascorbic acid (vitamin C) and d-alpha-tocopherol. J Am Acad Dermatol. 1998;38(1):45-48. Fuchs J, Kern H. Modulation of UV-light-induced skin inflammation by D-alpha-tocopherol and L-ascorbic acid: a clinical study using solar simulated radiation.

Free Radic Biol Med. 1998;25(9):1006-1012. Garcia-Doval I, LeCleach L, Bocquet H, Otero XL, Roujeau JC. Toxic epidermal necrolysis and Stevens-Johnson syndrome: does early withdrawal of causative drugs decrease the risk of death? Arch Dermatol. 2000;136(3):323-327. Garcia-Porrua C, Gonzalez-Gay MA, Vazquez-Caruncho M, et al. Erythema nodosum: etiologic and predictive factors in a defined population. Arthritis Rheum. 2000;43(3):584-592. Geria AN, Holcomb KZ, Scheinfeld NS. Necrolytic acral erythema: a review of the literature. Cutis. 2009;83(6):309-14. Grant WB, Holick MF. Benefits and requirements of vitamin D for optimal health: a review. Altern Med Rev.

2005 Jun;10(2):94-111. Review. Halliday GM, Yuen KS, Bestak R, Barnetson RS. Sunscreens and vitamin E provide some protection to the skin immune system from solar-simulated UV radiation. Australas J Dermatol. 1998;39(2):71-75. Hu JJ, Cui T, Rodriguez-Gil JL, et al. Complementary and alternative medicine in reducing radiation-induced skin toxicity. Radiat Environ Biophys. 2014;53(3):621-6. Jonas WB, Jacobs J. Healing with Homeopathy: The Doctors' Guide. New York, NY: Warner Books; 1996:263-265. Katiyar SK. Skin photoprotection by green tea: antioxidant and immunomodulatory effects. Curr Drug Targets Immune Endocr Metabol Disord. 2003 Sep;3(3):234-42. Review. Katiyar SK, Matsui MS, Elmets CA, Mukhtar H.

Polyphenolic antioxidant (-)-epigallocatechin-3-gallate from green tea reduces UVB-induced inflammatory responses and infiltration of leukocytes in human skin. Photochem Photobiol. 1999;69(2):148-153. Khanna VJ, Shieh S, Benjamin J, et al. Necrolytic acral erythema associated with hepatitis C: effective treatment with interferon alfa and zinc. Arch Dermatol. 2000;136(6):755-757. Khoury JG, Goldman MP. Use of light-emitting diode photomodulation therapy to accelerate resolution of post-intense pulsed light (IPL) erythema. J Cosmet Dermatol. 2008;7(1):30-4. Lee J, Jiang S, Levine N, Watson RR. Carotenoid supplementation reduces erythema in human skin after simulated solar radiation exposure. Proc Soc Exp Biol Med. 2000;223(2):170-174. Martinez AE, Atherton DJ.

High-dose systemic corticosteroids can arrest recurrences of severe mucocutaneous erythema multiforme. Pediatr Dermatol. 2000;17(2):87-90. Mert A, Kumbasar H, Ozaras R, Erten S, Tasli L, Tabak F, Ozturk R. Erythema nodosum: an evaluation of 100 cases. Clin Exp Rheumatol. 2007;25(4):563-70. Murray M. Encyclopedia of Nutritional Supplements. Rocklin, CA: Prima Publishing; 1996:320-335. Oresajo C, et al. Protective effects of a topical antioxidant mixture containing vitamin C, ferulic acid, and phloretin against ultraviolet-induced photodamage on human skin. J Cosmet Dermatol. 2008;7(4):290-7. Ozcan H, Seyhan M, Yologlu S. Is metronidazole 0.75% gel effective in the treatment of seborrhoeic dermatitis?

A double-blind, placebo controlled study. Eur J Dermatol. 2001;17(4):313-6. Passarini B, Infusino SD. Erythema nodosum. G Ital Dematol Venereol. 2013;148(4):413-7. Requena L, Sanchez Yus E. Erythema Nodosum. Dermatologic Clinics. 2008;26(4). Reuter J, Jocher A, Hornstein S, Monting JS, Schempp CM. Sage extract rich in phenolic diterpenes inhibits ultraviolet-induced erythema in vivo. Planta Med. 2007;73(11):1190-1. Reuter J, Jocher A, Stump J, Grossjohann B, Franke G, Schempp CM. Investigation of the anti-inflammatory potential of Aloe vera gel (97.5%) in the ultraviolet erythema test. Skin Pharmacol Physiol. 2008;21(2):106-10.

Schwartz R, Nervi S. Erythema Nodosum: A Sign of Systemic Disease. Am Fam Phys. 2007;75(5). Sies H, Stahl W. Nutritional protection against skin damage from sunlight. Annu Rev Nutr. 2004;24:173-200. Review. Sinclair SA, Reynolds NJ. Necrolytic migratory erythema and zinc deficiency. Br J Dermatol. 1997;136(5):783-785. Stahl W, Heinrich U, Jungmann H, Sies H, Tronnier H. Carotenoids and carotenoids plus vitamin E protect against ultraviolet light-induced erythema in humans. Am J Clin Nutr. 2000;71(3):795-798. Stern RS. Improving the outcome of patients with toxic epidermal necrolysis and Stevens-Johnson syndrome. Arch Dermatol. 2000;136(3):410-411.

Stupica D, Lusa L, Ruzic-Sabljic E, Cerar T, Strle F. Treatment of erythema migrans with doxycycline for 10 days versus 15 days. Clin Infect Dis. 2012;55(3):343-50. Taylor SC, Averyhart AN, Heath CR. Postprocedural wound-healing efficacy following removal of dermatosis papulosa nigra lesions in an African American population: a comparison of a skin protectant ointment and a topical antibiotic. J Am Acad Dermatol. 2011;64(3 Suppl):S30-5. Vickers AJ. Independent replication of pre-clinical research in homoeopathy: a systematic review. Forsch Komplementarmed. 1999;6(6):311-320. Webb AR, Engelsen O. Ultraviolet exposure scenarios: risks of erythema from recommendations on cutaneous vitamin D synthesis. Adv Ex Med Biol. 2014;810:406-22.

Alternative Names Pediatric Erythema Toxicum: Background, Pathophysiology, Epidemiology Pediatric Erythema Toxicum Author: Elizabeth Arrington, MD; Chief Editor: Dirk M Elston, MD more... Share Overview Background Erythema toxicum neonatorum (ETN) is a benign, self-limited, asymptomatic skin condition that only occurs during the neonatal period. [ 1 , 2 , 3 , 4 ] The eruption is characterized by small, erythematous papules, vesicles, and, occasionally, pustules. The lesions are usually surrounded by a distinctive diffuse, blotchy, erythematous halo. Individual lesions are transitory, often disappearing within hours and then appearing elsewhere on the body. See the image below. A 5-day-old newborn with erythematous papules with surrounding indistinct blotchy erythema visible on the abdomen. Image courtesy of Jining I. Wang, MD. See 13 Common-to-Rare Infant Skin Conditions , a Critical Images slideshow, to help identify rashes, birthmarks, and other skin conditions encountered in infants. Next: Pathophysiology The underlying pathophysiology is uncertain.

Although the initial description of toxic erythema of the newborn is attributed to the 15th century physician Bartholomaeus Metlinger, this neonatal cutaneous eruption was recognized before the time of ancient Mesopotamia. [ 5 ] Ancient Mesopotamian physicians believed this eruption to be "nature's method of cleansing the child of impure blood of the mother." In A Treatise on the Theory and Practice of Midwifery, the 18th century English physician William Smellie attributed the condition to "the costiveness of the child when the meconium hath not been sufficiently purged off." The characteristic presence of eosinophils within the lesions has led some investigators to attribute this condition to an allergy. Work by Eitzman and Smith suggested that eosinophilia is part of the normal spectrum of the nonspecific inflammatory response in the neonate. [ 6 ] This hypothesis is supported by cases in which premature neonates have infrequent eruptions that resolve within a few weeks after birth when the neonatal immune response matures.

The etiology of erythema toxicum neonatorum remains uncertain; however, more recent hypotheses explaining the appearance of this eruption include the following: Relative, increased, ground-substance viscosity in neonatal skin, with associated trauma leading to eosinophilic inflammation Self-limited, acute, cutaneous, graft-versus-host reaction caused by maternal lymphocytes in the relatively immunosuppressed fetal circulation [ 7 ] An innate immunologic response to commensal microbes within hair follicle epithelium An inflammatory response mediated by various inflammatory mediators, including aquaporins, psoriasin, nitric oxide synthases Previous References Kanada KN, Merin MR, Munden A, Friedlander SF. A Prospective Study of Cutaneous Findings in Newborns in the United States: Correlation with Race, Ethnicity, and Gestational Status Using Updated Classification and Nomenclature. J Pediatr. 2012 Apr 10. [Medline] . Tarang G, Anupam V. Incidence of vesicobullous and erosive disorders of neonates. J Dermatol Case Rep. 2011 Dec 12. 5(4):58-63.

[Medline] . [Full Text] . Reginatto FP, Villa DD, Cestari TF. Benign skin disease with pustules in the newborn. An Bras Dermatol. 2016 Apr. 91 (2):124-34. [Medline] . Ghosh S. Neonatal pustular dermatosis: an overview. Indian J Dermatol. 2015 Mar-Apr. 60 (2):211. [Medline] . Lehndorff H. Bartholomaeus Metlinger. A fifteenth century pediatrician. Arch Pediatr. 1951 Jul. 68(7):322-33. [Medline] . Eitzman DV, Smith RT. The nonspecific inflammatory cycle in the neonatal infant. AMA J Dis Child. 1959 Mar. 97(3):326-34. [Medline] . Bassukas ID. Is erythema toxicum neonatorum a mild self-limited acute cutaneous graft-versus-host-reaction from maternal-to-fetal lymphocyte transfer?. Med Hypotheses. 1992.

38:334-338. [Medline] . Haveri FT, Inamadar AC. A cross-sectional prospective study of cutaneous lesions in newborn. ISRN Dermatol. 2014. 2014:360590. [Medline] . Carr JA, Hodgman JE, Freedman RI, Levan NE. Relationship between toxic erythema and infant maturity. Am J Dis Child. 1966 Aug. 112(2):129-34. [Medline] . Keitel HG, Yadav V. Etiology of Toxic Erythema. Erythema Toxicum Neonatorum. Am J Dis Child. 1963 Sep. 106:306-9. [Medline] . Jawade SA, Chugh VS, Gohil SK, Mistry AS, Umrigar DD. A Clinico-Etiological Study of Dermatoses in Pediatric Age Group in Tertiary Health Care Center in South Gujarat Region. Indian J Dermatol. 2015 Nov-Dec. 60 (6):635. [Medline] .

Saracli T, Kenney JA Jr, Scott RB. Common skin disorders in the newborn Negro infant. Observations based on the examination of 1,000 babies. J Pediatr. 1963 Mar. 62:359-62. [Medline] . Liu C, Feng J, Qu R. Epidemiologic study of the predisposing factors in erythema toxicum neonatorum. Dermatology. 2005. 210(4):269-72. [Medline] . O'Connor NR, McLaughlin MR, Ham P. Newborn skin: Part I. Common rashes. Am Fam Physician. 2008 Jan 1. 77(1):47-52. [Medline] . Morgan AJ, Steen CJ, Schwartz RA, Janniger CK. Erythema toxicum neonatorum revisited. Cutis. 2009 Jan. 83(1):13-6. [Medline] . [Guideline] New York State Department of Health. Dermatologic manifestations. New York State Department of Health. 2004.

[Full Text] . Media Gallery A 5-day-old newborn with erythematous papules with surrounding indistinct blotchy erythema visible on the abdomen. Image courtesy of Jining I. Wang, MD. of 1 e.hormone | Human Effects Human Effects References Thousands of chemicals first made to improve our lives have spread unchecked to every corner of the world, polluting oceans, mountains, polar regions, tropics, wildlife, and people. Moved about by wind, water, and animals, the chemicals, and sometimes their more harmful breakdown products, contaminate soil, water, plants, people, and animals on every continent. CAPTION: Synthetic chemicals pollute every part of our planet, including this coastal redwood forest. CREDIT: Marc Hoshovsky Some of these ubiquitous chemicals, along with natural plant compounds called phytochemicals, can interact with the endocrine system, especially during critical developmental stages. These endocrine disrupting chemicals (EDCs) interfere by mimicking, blocking, or altering hormones and their signaling systems. Hormones work with the immune and nervous systems to regulate growth, reproduction, metabolism, immunity, cognition, and behavior. click here to read more about Phytoestrogens...

What's the fuss? Altering hormone signals can change how the body works and may lead to health problems. Some people speculate that EDCs may be linked to many health concerns, such as cancer, diabetes, obesity, learning disabilities and behavior changes. Solid evidence linking EDCs with these kinds of effects is lacking, but increasing anecdotal evidence suggests there might be something to the claims. However, studies of cell cultures, laboratory animals, wildlife, and accidentally exposed humans do show EDCs can cause a wide range of reproductive, developmental, growth, and behavior problems. The most attention has been given to those compounds that produce estrogenic, androgenic, antiandrogenic, and antithyroid actions. Less is known about interactions with other hormones and possible effects on immunity (infections), metabolism, (obesity), the brain (intelligence, behavior), the heart, the lungs, and multiple generations. But effects vary. Distinct health effects can occur in different organs and at different life stages. Exposed adults may not show ill effects.

But, fetuses and embryos, whose growth and development are highly controlled by the endocrine system, are more vulnerable to exposure and may suffer overt or subtle lifelong health and/or reproductive abnormalities (Bern 1992). Prebirth exposure, in some cases, can lead to permanent alterations and adult diseases. For example, testicular cancer in young men takes root before birth during fetal development. Certain cancers and uterine abnormalities in women are associated with exposure to DES in the womb. In another case, phthalates in pregnant women’s urine was liked to subtle, but specific, genital changes in their male infants – a shorter, more female-like anal-genital distance and associated incomplete descent of testes and a smaller scrotum and penis (Swan et al. 2005). The ubiquitous compounds, found in plastics and cosmetics, are known to block the androgens that control development of the normally longer male anal-genital distance. back to top Biomonitoring: They’re in Us, Too We all carry a heavy mix of hormonally active compounds within us.

Synthetic contaminants are passed to us by our parents and picked up at home, at work, in the car, and outside via skin, while breathing, and through food and drink. We accumulate the longer-lasting chemicals (the PCBs, dioxins, and organochlorine pesticides) just by living, store them in fat, and often pass them on to our children through the womb and breast milk. Our exposure to other widely used but less persistent toxic chemicals - such as phthalates, phytochemicals, hormonal drugs, and additives like bisphenol A - is also widespread and occurs throughout life. back to top High Dose Exposures: Known Human Effects Two examples where people were exposed to very high doses illustrate that EDCs can affect humans health: the drug diethylstilbestrol (DES) and the accidental exposure of the population of Seveso, Italy to dioxin (TCDD or tetrachloro-dibenzo-p-dioxin). DES, a strong synthetic estrogen banned since the 1970s, was given to pregnant women for about 40 years to prevent miscarriages. It was not until the daughters were grown that the negative side effects became known.

Daughters of mothers who took the synthetic estrogen during pregnancy have higher rates of reproductive problems, reproductive cancer (vagina, cervix) and malformed reproductive organs (uterus, cervix) (Noller et al. 1990). Sons may also face higher rates of malformed or small penises, undescended testicles and abnormal sperm (Gill et al. 1976). However, there is no evidence of reduced fertility in DES sons. Mice studies confirmed that DES caused the reproductive problems and certain cancers (including the rare rete-testicular cancer in males). More recent animal studies show multigenerational effects and find granddaughters and sons may also be affected (CDC 2005b). DES is not only a potent estrogen, similar in strength to the natural estrogen estradiol, but it also has the unique ability to concentrate in target tissues, such as the reproductive tracts of birds, reptiles and other animals, during development and cause abnormalities. This drug serves as an example of what potent estrogenic compounds can do and may illustrate the health effects that other environmental estrogens can produce.

The Seveso, Italy, dioxin event, though not the only known case, is probably the most studied population following a chemical disaster in the world. On a quiet July day in 1976, a cloud of industrial chemicals rose in the air from the Industrie Chimiche Meda Societa Azionaria chemical plant and engulfed the unsuspecting town and region. The chemicals, a mix of herbicide ingredients, contained about 30 kilograms (66 pounds) of dioxin, a long-lived, hormonally active, cancer causing poison. It took hours for the first burns to appear on children, days for animals to die, months before the classic dioxin-associated skin disease chloracne developed, and years before the more insipid effects were found. Decades later, people’s health is still affected. Residents have been poked, prodded, and studied since the explosion and continue to be part of research to determine the long-range effects from a heavy dose of a strong pollutant. Studies evaluating cancers, endometriosis, reproduction, immune function, menopause, miscarriages, and other parameters are numerous. Some effects have not correlated with the dioxin.

Other effects have taken years to manifest. For example, a significant increase in breast cancer risk with higher dioxin exposures was found more than 10 years after initial exposure (Warner 2002) and life-long immune system problems continue with lowered ability to resist disease. back to top Other Exposures: Some Examples Human health is affected by direct exposure to large doses of EDCs. Less clear are effects from everyday exposures to complicated mixes of pollutants. Circumstantial evidence suggests there might be reason to be worried. Below are some examples of less cut and dried cases of possible human health effects from various sources and unclear doses of exposure. Phytochemicals Plant compounds can interact with hormone receptors and produce mainly estrogen-like effects. The results of these disruptions are not always agreed upon. For example, phytoestrogens, such as genistein, in soybeans and soy products has been shown to provide benefits – cancer prevention, heart protection - as well as risks - mainly cancers and reproductive troubles. Most concern surrounds effects on infants fed only soy-based formula. back to top Concern is Warranted Although large exposures produce known effects, impacts from long term, low level adult exposure is less clear and more controversial.

It’s the kids, though, that cause the most concern. Because, even more unknown is the prospect that developing embryos, fetuses, infants, and children, whose growth and development is highly controlled by endocrine signals, may be more vulnerable to exposure at certain times and may suffer lifelong effects from those encounters. Although the 1993 global assessment found insufficient data to reach concrete conclusions about impacts to human health, it concluded there is sufficient evidence to warrant concern (IPCS 2002). back to top References Carlsen E, Giwercman A, Keiding N, and Skakkebaek NE. 1992. Evidence for decreasing quality of semen during past 50 years. British Medical Journal 305:609-613. CDC (Centers for Disease Control and Prevention). 2005a. Third National Report on Human Exposure to Environmental Chemicals. Atlanta, GA:Department of Health and Human Services. Available: (accessed 1 February 2006). CDC (Centers for Disease Control and Prevention). 2005b. DES Update. Available: (accessed 28 November 2005).

Clotfelter ED, Bell AM, and Levering KR. 2004. The role of animal behaviour in the study of endocrine-disrupting chemicals. Animal Behaviour. 68(4):665-676. Dewailly E, Ayotte P, Bruneau S, Gingras S, Belles-Isles M, and Roy R. 2000. Susceptibility to infections and immune status in inuit infants exposed to organochlorines. Environmental Health Perspectives 108:205-211 Duty S, Silva M, Barr D, Brock J, Ryan L, Chen Z, Herrick R, Christiani D, and Hauser R. 2003. Phthalate exposure and human semen parameters. Epidemiology 14:269-277. Fisch, H. and Goluboff. 1996. Geographic variations in sperm counts: A potential cause of bias in studies of semen quality. Fertility and Sterility 65:1044-1046.

Guillette EA, Meza MM, Aquilar MG, Soto AD, and Idalia Enedina Garcia, IE. 1998. An anthropological approach to the evaluation of preschool children exposed to pesticides in Mexico. Environmental Health Perspectives 106:347-353. Hauser R, Chen Z, Pothier L, Ryan L, and Altshul L. 2003. The relationship between human semen parameters and environmental exposure to polychlroinated biphenyls and p,p’-DDE. Environmental Health Perspectives 111:1505-1511. Hunt PA, Koehler KE, Susiarjo M, Hodges CA, Ilagan A, Voigt RC, Thomas S, Thomas BF, and Hassold TJ. 2003. Bisphenol A exposure causes meiotic aneuploidy in the female mouse. Current Biology 13:546-553. IPCS (International Programme on Chemical Safety). 2002. Global Assessment of the State-of-the-Science of Endocrine Disruptors. WHO/PCS/EDC/02.2. Eds.

Damstra T, Barlow S, Bergman A, Kavlock R, and Van Der Kraak G. Geneva, Switzerland: World Health Organization. Available: (accessed 28 November 2005). Mackenzie CA, Lockridge A, and Keith M. 2005. Declining sex ratio in a First Nation community. Environmental Health Perspectives 113:1295-1298. Mocarelli, P, PM Gerthoux, E Ferrari, DG Petterson, SM Kieszak, P Brambilla, N Vincoli, S Signorini, P Tramacere, V Carreri, EJ Sampson, WE Turner and LL Needham. 2000. Paternal concentrations of dioxin and sex ratio of offspring. The Lancet 355:1858-1863. Safe S. 1995. Do environmental estrogens play a role in development of breast cancer in women and male reproductive problems? Human and Ecological Risk Assessment 1(2):17-23. Sharpe, R.M. and Shakkebaek. 1993.

Are oestrogens involved in falling sperm counts and disorders of the male reproductive tract? Lancet 341:1392-1395. Sugiura-Ogasawara M, Ozaki Y, Sonta S, Makino T, and Suzumori K. 2005. Exposure to bisphenol A is associated with recurrent miscarriage. Human Reproduction 20:2325-2329. Swan SH, Elkin EP, and Fenster L. 1997. Have sperm densities declined? A reanalysis of global trend data. Environmental Health Perspectives 105:1228-1232. Swan S, Elkin E, and Fenster L. 2000. The question of declining sperm density revisited: An analysis of 101 studies published 1934-1996. Environmental Health Perspectives 108:961-966. Swan S, Brazil C, Drobnis E, Liu F, Kruse R, Hatch M, Redmon J, Wang C, Overstreet J, and Study for Future Families Research Group.

2003a. Geographic differences in semen quality of fertile US males. Environmental Health Perspectives 111:414-420. Swan S, Kruse R, Liu F, Barr D, Drobnis E, Redmon J, Wang C, Brazil C, Overstreet J, and Study for Future Families Research Group. 2003b. Semen quality in relation to biomarkers of pesticide exposure. Environmental Health Perspectives 111:1478-1484. Swan, SH, Main KM, Liu F, Stewart SL, Kruse RL, Calafat AM, Mao CS, Redmon JB, Ternand CL, Sullivan S, and Teague JL. 2005. Decrease in anogenital distance among male infants with prenatal phthalate exposure. Environmental Health Perspectives 113:1056-1061. Warner M, Eskenazi B, Mocarelli P, Gerthoux PM, Samuels S, and Needham L. 2002. Serum dioxin concentrations and breast cancer risk in the Seveso Women’s Health Study.

Environmental Health Perspectives 110:625-628. Zala SM and DJ Penn DJ. 2004. Abnormal behaviours induced by chemical pollution: a review of the evidence and new challenges. Animal Behaviour. 68(4):649-664. What Is Lupus and How Does It Affect the Body | S.L.E. Lupus Foundation What Is Lupus and How Does It Affect the Body From the 2012 Lupus Education Series Understanding what lupus is as an autoimmune disease and how it affects the body was the focus of a presentation by Dr. Laura Geraldino, MD at Columbia Presbyterian Medical Center. Dr. Robert Winchester followed her presentation with an open question and answer session. Laura Geraldino, MD – What is Lupus? Addressing the packed room, Dr. Geraldino started the night off with simple explanation of how the immune system works to lay the foundation for understanding how it malfunctions in people with lupus. An Autoimmune Disease The immune system protects the body from foreign substances and infection.

But in an autoimmune disease like lupus, the immune system attacks the body.SLE is characterized by auto-antibodies, meaning that the antibodies attack the “self” SLE is unpredictable, varying in how it affects every person. It cannot be cured but controlled Illnesses occur when the body tissues are attacked by its own immune system. Manifestations of Lupus The American College of Rheumatology provides the following criteria for diagnosing lupus: Malar rash — the classic butterfly rash on the face crossing the nose and cheeks that can be very subtle or very noticeable Discoid rash — round lumps on the skin that appear most often on the scalp and ears Oral lesions — sores in the mouth, often on the roof of the mouth Arthritis — joint pain, mostly in the hands and knees Serositis — inflammation around the lungs, heart and abdomen Lupus Pleuritis — chest pain with breathing, fluid around the lungs Lupus Nephritis — kidney disease varies widely from person to person; biopsy is used to determine the type and extent of damage Lupus in the Nervous System — varies widely, affecting the brain and nervous system. Nineteen related physical and emotion syndromes include anxiety, headaches, seizures and memory loss.

Positive ANA — Blood test used to screen for lupus. Almost everyone who has lupus will have a positive ANA test, but not everyone who has a positive ANA test has lupus. Other Manifestations Fatigue — very common and can be very debilitating Fever — can be caused by lupus or by something unrelated so needs to be checked by doctor Hair loss — can be thinning hair or patches Purple fingers in the cold — painful Blood clots Consequences People with lupus are at greater risk for health issues and death, making early diagnosis and close monitoring essential! However, the outlook is much more positive for people with lupus than it was 50 years ago. Bio: Laura Geraldino Pardilla, MD Dr. Geraldino specializes in autoimmune diseases, especially Systemic Lupus Erythematosus (Lupus) and Rheumatoid Arthritis. She heads up the Lupus Clinic at Columbia University Medical Center. Working in this predominantly Hispanic neighborhood made her notice and develop an interest for lupus as an autoimmune disease with increased frequency and severity in this ethnic group. Having completed her residency in Internal Medicine at State University of New York Upstate Medical University, Syracuse, NY, Dr.

Geraldino went on to complete a second fellowship in musculoskeletal ultrasound at USSONAR Cooper Health System. Robert Winchester, MD – Who Gets Lupus and Why? Dr. Winchester’s approach was quite different – instead of giving a presentation, he asked the audience for questions relating to who gets lupus and why it develops. Following is a sampling of the very lively Q&A “conversation” between Dr. Winchester and attendees. How is lupus a genetic disease? It is not inherited in a simple fashion, like for example eye color, but is the result of at least 40-50 genes each of which contribute a part of the risk for lupus. However, these are not abnormal genes in the sense that the gene for sickle cell disease makes an abnormal hemoglobin in the red cell. Each gene independently appears to be beneficial, perhaps contributing to a stronger and more vigorous immune response. However it looks that when we inherit too many of these genes they “gang up” and result in the abnormal immune response that results in lupus. Our knowledge of these genes comes from the Human Genome Project, where scientists have sequenced DNA, which led to the identification of all of the different genes.

Research work supported by the Lupus Research Institute has helped help show that these genes are important to developing lupus and that they work in some part of the immune system work; some may help in some circumstances but have a harmful effect in others. We are going towards personalized medicine which would allow us to identify specific genes that predict risk for lupus for some people. How do you differentiate among all the autoimmune diseases to determine that a person has lupus? Good question as there are over 100 autoimmune diseases and many of the symptoms overlap. But we look for a pattern of symptoms that indicate the processes going on. For instance, Sjogren’s and lupus have many similar clinical and laboratory features such as a positive ANA, but Sjogren’s symptoms typically affect the eyes and the ability to swallow dry crackers because of the lack of saliva, while lupus does not. So when a patient describes those symptoms, we can begin to hone in on where in the body the disease is targeting that indicate which type of autoimmune disease may be responsible. How does lupus develop? Lupus does not just happen over a few hours or days.

Recent research work shows years before you develop the symptoms of lupus, those autoantibodies were already there in your body and were attacking your “self” just a little so you still felt perfectly healthy. This is considered a pre-clinical, pre-lupus state and it may offer a window of time before the disease symptoms starts when we may be able to intervene to change the course of this autoimmune response and block development of the clinical disease. We are just learning about this and about the genes that are responsible, but with the groundbreaking research going on now, within five years, we may be able to modify or nullify the genes that can cause lupus. We hope we can put the genie back in the bottle to maintain or revert back to this pre-lupus state. Even now, if there is a strong family history of lupus, we might consider starting a person who is found to have a positive ANA and other certain autoantibodies on an anti-malarial drug like hydroxychloroquine to try to prevent the clinical disease of lupus from developing.

Also, if we know a person as a family history so may be predisposed to lupus, we would recommend ways to reduce their risk by cutting down on lifestyle factors known to trigger lupus such as avoiding direct sunlight and not smoking. Why don’t we hear much about research in lupus? As you know, lupus is an extremely difficult and challenging disease. There has always been research going on, but now there is an explosion of research in the field and we expect revolutionary changes in how the disease is diagnosed and treated within about five years. And since lupus is an autoimmune disease among at least 100 others, advances in one disease like type-1 diabetes can be an advance in another autoimmune disease like lupus. So some research that was not initially targeted to lupus in fact produces knowledge that advances our understanding of lupus. Is lupus caused by genetics or environment? Both. It is genetic in the sense that you always had the predisposition to make the antibodies that cause lupus. But these predisposing genes are influenced by environmental events, such that an infection or smoking can bring it out. Does nutrition have any impact on lupus? There is no evidence that food impacts lupus.

However, there is research looking at whether chemical additives in foods could have a negative effect. Also studies have indicated that below normal levels of Vitamin D may raise the risk for lupus while taking the vitamin might reduce the severity of the disease. Research has also suggested that small amounts of alcohol might be beneficial, perhaps to relax the body and alleviate stress. But not too much! Does vaccination impact lupus? There is no clear answer yet. But research has indicated that there is no relationship between immunization and a greater likelihood of developing lupus or a greater risk for developing a flare. In fact, immunizations like the flu or pneumococcal vaccine are generally recommended for people with lupus because you are immunodeficient. In lupus, immunodeficient or immunocompromised means that while the lupus is causing your body’s antibodies to attack your own body they are distracted from attacking the invader such as the flu virus. Vaccination can stimulate your body’s immune system in a positive way to create antibodies that will attack the virus specifically. Bio: Robert Winchester, MD Dr. Winchester is a Professor of Pediatrics, Pathology, and Medicine at Columbia University and has spent his career studying the autoimmune diseases and the genetic basis of those who develop them.

He identified various allelic forms of HLA-DR, and was the first to show that the genetic susceptibility to systemic lupus differed from that associated with rheumatoid arthritis. Many of Dr. Winchester’s discoveries in the genetic factors influencing lupus have been made possible by grants from the Lupus Research Institute Erythema Multiforme Erythema Multiforme Outlook A rash is a rash is a rash, right? Not quite! The target-shaped spots of erythema multiforme might be unlike any other rash you've ever seen. About Erythema Multiforme Erythema multiforme is a hypersensitivity reaction to an infection or, in some cases, a medicine. This reaction causes red, target-shaped or "bulls-eye" patches or sores on the skin. The rash usually starts off looking like pink or red blotches that develop over a few days into round shapes that look like targets (with red, pink, and pale rings). They sometimes have blisters or scabs in the center. The rash usually begins on the arms, hands, legs, and feet, but you might also find it on the face, neck, and body.

In more severe cases (called erythema multiforme major), it also can affect the lips and inside of the mouth. One of the characteristics of an erythema multiforme rash is that it develops on both sides of the body. So a kid who gets it on one leg probably will get it on the other leg too. Kids usually complain that the rash itches and may even burn. As the rash goes away, it can turn a brownish color. The rash, which usually develops quickly, might be the only sign that a child has the condition. However, sometimes kids also may feel tired or have: mouth sores or blisters mild ache in joints and muscles Causes Most cases of erythema multiforme are believed to be a reaction to an infection that causes the body's immune system to damage the skin cells. More than half of cases are associated with the herpes simplex virus, the virus that causes cold sores . But bacteria like mycoplasma, fungi, and other viruses are also triggers for the rash. Erythema multiforme can happen after someone takes certain medicines, although this is a less likely cause than an infection.

Some of the medicines that can trigger a reaction are: seizure drugs, like phenytoin nonsteroidal anti-inflammatory drugs, including ibuprofen antibacterial drugs, like sulfonamides penicillin and other antibiotics Also, some cases happen after a child has an immunization, such as the tetanus-diphtheria-acellular pertussis (Tdap) or hepatitis B vaccines. The rash is not contagious, so cannot be passed from one person to another. continue Diagnosis Doctors usually recognize erythema multiforme just by looking at it. To help figure out what caused it, the doctor will ask about any recent infections the child has had and any medicines he or she is taking. Sometimes, the cause isn't known. Treatment Erythema multiforme goes away on its own without treatment. In many cases, though, the doctor will try to treat whatever caused a child to have the reaction. So, if a bacterial infection is thought to be behind the rash, the doctor may recommend that a child take an antibiotic. If a medicine is the likely culprit, the doctor probably will have a child stop taking it and replace it with another medication, as needed.

To help make kids feel better, doctors may recommend: putting cool compresses on the rash using acetaminophen , antihistamines, or topical creams to ease itchiness or soreness for more severe cases, using a steroid medicine for a few days Although these treatments provide relief, they do not shorten the duration of the rash. In severe cases, hospital treatment is needed and a person might get IV (intravenous, given into a vein) medicine, such as antibiotics or steroids. Outlook Most kids who get erythema multiforme have no long-term effects. The rash usually goes away in 1 to 2 weeks, but can last as long as 4 weeks. It doesn't cause scarring, but in some kids might leave darker spots on the skin for a few months. An erythema multiforme rash may come back again (recur) after going away, especially if a child is re-exposed to whatever caused the initial outbreak. If the herpes simplex virus is causing repeated episodes of erythema multiforme, a doctor may prescribe a daily antiviral medicine to prevent recurrences.

Question: Erythema affects which part of the human body?
Answer: Skin